Toymaker Television

Daily content for the geek and DIYer

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How to use the TTL8 board!

The TTL8 board is a new board that we have recently put out on Tindie ( and not only is it small and compact, it’s quite useful for turning on and off low current loads such as LEDs.

The board consists of a shift register, 8 leds (or not), and headers for input into the shift register, output from the shift register, and header space for daisy chaining for multiple TTL8 boards.  If you’ve ever worked with the 74hc595 shift register (or any shift register in general), the number of wires required to get one of those bad boys working is a pretty prohibitive pain in the butt.  For example, see the following:


I’m anti clusters of wires.  So the board takes all of those wires and puts them into a 5/8” x 1-1/8” footprint.  As a stand-alone board, for just LED indication, you only need your microcontroller and 5 wires going to the Port In side: (from left to right) Power, GND, Latch, Clock, Serial.


Most of the microcontrollers I work with use 3.3v.  And you can certainly connect the TTL8 board to the microcontroller, or you can, if you’re daisy chaining a bunch of TTL8 boards, use the power and gnd header on the bottom left with greater current capabilities.  Just note that voltage-wise, your uC voltage needs to be the same as that provided to the board. So if your microcontroller works off of 3.3v, provide your TTL8 board with 3.3v.

If you want the shift register to drive 8 other items, or even 8 LEDs that aren’t attached to the board, that’s how you’d use 0-7 header.  The shift register is connected to all 8 of the pins and can drive whatever you’d like - within current limits of the shift register of course.

Whisker uses this board as a debug board - so if you want to check if your input device is actually working as expected, or sending signals as desired, you can have it light up the LEDs.



So this is of course using the Propeller microcontroller.  I used the demo board and programmed it in Spin.  In the main body of the program, the propeller sets the pins sending out Latch, Clock, and Serial as outputs.  It then repeatedly monitors to see whether a key’s been pressed.  If it has, it puts it into register dirb. 

And repeating from index 0 to 7, it spits out via serial what key has been pressed in register dirb.  If you had 4 TTL8 boards chained together, you’d repeat index 0 to 31.

So it spits out the serial, then it outputs a 1 on the clock line to bring it high, then brings it low to signify that a bit has been set, and that the next bit can be set in the shift register.  Then after all index values have been gone through, the latch is set high and low again.  This feeds it out to the indicator leds, or to whatever you’re driving.

And that’s the TTL8 board!  Again it’s available: and if you have any questions, let us know!


Filed under ttl8 board ttl8 module shift register 74hc595 tymkrs tindie propeller shift register and propeller spin driving leds with shift register

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Going Postal: Clacks Towers - Step 2: Sending Binary

So the last post, I was able to at least test to see that the keyboard was working properly.  Today I wanted to work more on trying to get the keyboard sending information to LEDs.

So connected I have the keyboard to the Parallax Demo Board.  Then I have an NPN8 kit (one of our new kits) which allows you to send signals through a shift register (serial to parallel) and output onto 8 separate channels - in this case LEDs!  

The NPN8 Kit has 5 connections on one side (from right to left) : Power, GND, Clock, Latch, Serial (In the Port In section).  Pins 0-7 on the Port In side connect to the emitters of the transistors and Pins 0-7 on the Port Out side connect to the collectors of the transistors.


So from right to left in Port In: 3.3V, Ground, and put Clock, Latch, and Serial on Propeller Demo Board pins 2, 1, and 0 respectively (just because of how the wiring went). 

Using the Tymkrs Shift Me example code (another kit), and with the help of Whisker, we shortened it and incorporated it into the keyboard code:


It essentially sets Latch, Clock, and Serial as outputs. Then looks at the keyboard.  If a key is pressed, the key’s information gets passed into variable Index as a long (32 bits).  I left a debug line there so that if you wanted to see your typing on the serial terminal, you could.

Then I directed the Propeller to examine this variable Index, specifically bits 0 to 7.  I then told it to send bits 0 to 7 out on Serial to the shift register. 

  • Note, remember shift registers (serial to parallel), take 8 bits in serially, and pass them out in a parallel fashion.  To do so, you send in a bit, the clock has to go high then low, rinse repeat.  When you are ready to release the stored inforation, the latch has to go high then low.

Then as mentioned before, I sent in a bit, set the Clock to high, then low. And after 8 bits, set the Latch to high, then low.  This process tells the shift register to release its stored bits.  So whatever you typed, essentially shows up on the LEDs!


The board above is a TTL8, another upcoming kit and allowed me to test with the LEDs, on the board, whether the keyboard was sending the correct information and whether the LEDs were lighting up appropriately.  The way it functions is pretty much the same as the NPN8.  Only difference is instead of driving 8 transistors which drive the LEDs, the TTL8 board drives the LEDs directly from the shift register. <— for more information on how shift registers work.

IT WORKS! Now for cosmetics!!!


Filed under tymkrs shift register npn8 ttl8 parallax keyboard parallax demo board parallax propeller spin keyboard and propeller

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Going Postal: Clacks Towers - Step 1: The keyboard

Of Terry Pratchett’s Discworld movies, I like Going Postal the most.  The story’s both interesting, hilarious, and they have fabulous technology - the clacks towers.  These are a system of semaphore towers capable of spreading messages 1 letter at a time.  

Instructables sent our hackerspace a bunch of LEDs and I thought it’d be a lot of fun if I made a semaphore tower with the LEDs for our hackerspace’s monthly build night.  But of course I wanted to make it easier to transmit messages, so I’ll be incorporating a keyboard into the project.

So I have a Parallax keyboard plugged into a Propeller Demo Board, and wanted to at least see that it worked.  Note the purple port below!


I went to the OBJ to look for a keyboard demo, and found one but it didn’t seem to do anything.  So I looked around a bit more and found .  There was some test code:


Which I put into PropTool.  I then opened up the serial terminal (Run —> Parallax Serial Terminal) and pressed enable.  I compiled the code on RAM and saw that as I typed letters, a red light appeared by the USB cable.  This was all well, but nothing was showing up on the serial terminal.  

So I looked for which COM port the keyboard was talking on (Run -> Identify Hardware) and saw it was a different COM than what was set on the serial terminal.  As soon as I changed the COM port on the serial terminal, it was golden!


Don’t forget to make sure your baud rate is 57600! 

The next step for me is to try to get the keyboard to send the binary of each letter out through our latest kit NPN8 to some LEDs!


Filed under ps2 keyboard and propeller propeller keyboard keyboard to serial terminal tymkrs

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Context is everything

Just as a follow-up to this article, I haven’t been through the ENTIRE process, but have certainly been witness to what it all involves.  Essentially after writing a paper, you send it off to a journal, who then chooses 3-4 reviewers from your field to review your paper.  They rip it to shreds, find what data still needs to be done, and then come back with their red pen telling you what’s what.  That’s called a peer-review.  And you either rebutt or you add on to your research to answer their questions.

The reason peer-review is important is because while YOU may be convinced about the results and what the results mean, your job as a scientist is to demonstrate proof to others who are equally qualified to analyze your data.  The peer reviewer is meant to make your data become above-reproach.

So it was interesting when I read this comment, in response to the article I’ve been reading through:

This team expressed quite a few concerns about the article, many of them which I have not vetted, but is worth considering because it largely considers the study negligent and over-exaggerating of its results.  It’s all because of context.  I’d advise you take some time to read through the answer, it’s pretty interesting and informative.

This also touches on why I think it’s interesting that this particular study, performed at a rather prestigious center, would send this sort of article to PLOS One as opposed to a more well known journal.  Because if indeed this data is sound and if the technique is sound, then it has fairly significant findings that a journal would be happy to pick up.  

The following is the peer review “About Us” for PLOS ONE: “Often a journal’s decision not to publish a paper reflects an editor’s opinion about what is likely to have substantial impact in a given field. These subjective judgments can delay the publication of work that later proves to be of major significance. PLOS ONE will rigorously peer-review your submissions and publish all papers that are judged to be technically sound. Judgments about the importance of any particular paper are then made after publication by the readership, who are the most qualified to determine what is of interest to them.”

I don’t know what kind of peer review this went through, but from the one review done by the commenter, it seems not enough.


Filed under the flip side tymkrs peer review plos one ritalin dopaminergic neuron dopaminergic system chronic ritalin

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Ritalin and Dopaminergic System Part 6

Following article courtesy of @lmcomie:

Sadasivan, S., Pond, B.B., Pani, A.K., Qu, C., Jiao, Y., & Smeyne R.J. (2012) Methylphenidate Exposure Induces Dopamine Neuron Loss and Activation of Microglia in the Basal Ganglia of Mice. PLOSONE, 7(3).

Last post about this article!  I finally found some time to go through the materials and methods.  So St. Jude Children’s Research Hospital was where this research was done.  The mice were 3 weeks old and maintained on a 12h light/dark cycle (this is normal).  Starting when they were 28 days (this is about young adulthood/just off weaning), they were given injectsion of saline, 1mg/kg or 10mg/kg Ritalin at 5pm - 1 hour before their active nocturnal phase at 6pm.

Doses were chosen sbased on previous studies in rodents suggesting that Ritalin doses of < 5mg/kg mirror those that are used in clinical practice, as opposed to recreational and narcoleptic use = dose of 10mg/kg.

Ritalin injections were given 5 days a week and at the end of the 12 weeks, the animals were allowed a washout period of a week.

After the week of washout, the mice were anesthetized and euthanized.  The method they describe is fairly common for brain analysis.  And then the brain was sliced to 10um thick for analysis.  I can’t tell if they had to count neurons by eye or not, but they mentioned using a “optical fractionator method” - it may be some sort of estimating tool developed with a specific microscope in mind.

For MPTP treatment, the final concentration was 5mg/ml and each animal was given 4 injections of 20 mg/kg MPTP - one every 2 hours for 8 hours.  All mice then stayed around for a week after the injections, before euthanization.

The rest of the article describes the methods they used for measuring mRNA and expression signals - unfortunately not my forte - but still a well documented method in many different studies.

I think one thing to note is that the n levels (number of subjects) that they tested throughout these experiments is relatively low compared to how many mice are usually put through an experiment.  The n numbers are anywhere from 3 to 8.  This is not very high.  IE. They’re using the results from 3 mice to come to this conclusion.  The research would have been much stronger had there been at least 10 mice per category.  The logistics, however, would have been difficult.  (Why? Cuz mice don’t like injections anymore than humans do)


Filed under tymkrs ritalin dopaminergic neuron methylphenidate chronic ritalin parkinsons methods

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Ritalin and Dopaminergic System Part 5

Ritalin and Dopaminergic System Part 5

Following article courtesy of @lmcomie:

Sadasivan, S., Pond, B.B., Pani, A.K., Qu, C., Jiao, Y., & Smeyne R.J. (2012) Methylphenidate Exposure Induces Dopamine Neuron Loss and Activation of Microglia in the Basal Ganglia of Mice. PLOSONE, 7(3).

The discussion section is like the summary section with a “why did we get the results we got” added in.  So if a lot of this looks familiar, it’s probably because it is!

Alright, so they do a study looking at the effects of an ADHD and Narcolepsy dose of Ritalin.  They found that giving both doses chronically makes dopaminergic neurons in the substantia nigra, a location in the brain involved in reward, addiction, and Parkinson’s, more susceptible to further stress.  And it does it by increasing the number of inflammatory factors that are activated/created and decreasing the factors that are usually responsible for creating new neurons, more dopamine, etc.

Specifically, they used a 3 month Ritalin schedule that spans the developmental period in mice and corresponds to the pre-adolescent through young adult period in humans, during which Ritalin’s usually used.

Usually Ritalin works by increasing the amount of dopamine and norepinephrine in the brain by blocking the proteins that take back dopamine and norepi once they’ve finished their actions.  In the study, they saw that there was a significant increase in dopamine levels at the ADHD dose, one that was not seen at the narcolepsy dose.  Other small doses that have been studied have also seen this increase in dopamine levels.  

The lack of change in dopamine at the higher level may be because of chronic dosing of the drug, or maybe some sort of compensatory change in the production of dopamine due to there being fewer neurons.  So they measured the ratio of dopamine to dopaminergic neurons.  Interestingly, when examined as a ratio, both the 1 and 10mg/kg doses showed a significant increase in the dopamine:neuron ratios - 150% in 1mg/kg and a 132% increase in 10mg/kg Ritalin.  This suggests that both doses increase dopamine levels, not just that of 1 mg/kg.

Of course, increased extracellular dopamine may be a problem.  Oxidation of dopamine can produce a whole bunch of superoxides and in turn radicals.  Neurotoxins abound!  And as mentioned before, they hypothesized that chronic Ritalin would cause the neurons to be more sensitive to a later stress.  So they gave MPTP, an agent that is known to induce oxidative stress (one that normally does not induce any stress on the particular strain of mouse they had).  They found that chronic exposure to both doses increased the sensitivity of the neurons to oxidative stress - based on the fact that both doses lost neurons when given Ritalin and MPTP as compared to saline.

They also found that there was a significant increase in Ritalin-induced microglia - so they think that perhaps, an increase in radical formation from increased dopamine levels + a neuroinflammatory response (increase in microglia) increases the sensitivity of the dopamine neurons to a later oxidative challenge.

They wanted to see if there were any specific explanations for why the neurons were more sensitive to oxidative stress after having been given Ritalin.  Through genetic analysis, they saw that there were a number of genes that changed their level of expression after both 1 and 10mg/kg doses.  These were mostly related to inflammation and cell damage and repair pathways.  They found a decrease in expression of genes involved in dopamine synthesis and handling - again after both doses of Ritalin.

They found that short term exposure to higher doses of Ritalin increased the expression of inflammatory genes in the striatum.  Surprisingly they did not find an increase in inflammatory gene expression after chronic administration of Ritalin, though there was still an increase in activated microglia.  This suggests that sometime during the course of the chronic Ritalin, there may be some sort of repression of inflammatory gene expression.

Unknown if the gene repression after chronic treatment with Ritalin is permanent or if it can be later re-induced.  If this is the case, then the activated microglia may potentially play a modulatory role in inducing oxidative stress.  Or perhaps the microglia that are activated are not able to return to their pre-inflamed state.

So all together, this study suggests that chronic Ritalin in mice results in a reduced expression of neurotrophic factors (creation/healing), increased inflammation, and a loss of dopamine neurons.

Tomorrow, the methods! (Arguably one of the most important sections)


Filed under tymkrs dopaminergic neurons ritalin chronic ritalin neuroinflammation methylphenidate mrna expression neurotrophins dopamine

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Ritalin and Dopaminergic System Part 4

Following article courtesy of @lmcomie:

Sadasivan, S., Pond, B.B., Pani, A.K., Qu, C., Jiao, Y., & Smeyne R.J. (2012) Methylphenidate Exposure Induces Dopamine Neuron Loss and Activation of Microglia in the Basal Ganglia of Mice. PLOSONE, 7(3).

The wording keeps getting more and more jargony! Please be sure to check out parts 1, 2, and 3

Alterations in Gene Expression following Acute and Chronic MPH Exposure in SN:

They wanted to see whether there were any changes to gene expression and see what the genes were for.  They found that expression of 115 genes had changed between saline and the 1mg/kg Ritalin dose and expression of 54 genes had changed between saline and the 10mg/kg Ritalin dose.  Of these genes, 23 were expressing differently between the lower and higher Ritalin dose.

Since the larger changes in neuronal number and microglia (cells involved in fixing the brain after traumatic brain injury) occurred with the higher dose, they wanted to look at the gene expression in mice with only this dose.  They looked at specific genes associated with basal ganglia toxicity (note: the basal ganglia consists of structures involved in control of voluntary motor movements, procedural learning, routine behaviors or “habits”, eye movements, cognition and emotion) including:

  • brain derived neurotropic factor (bdnf): support survival of neurons and growth of new ones
  • glial derived neurotopic factor (gdnf): promotes survival and differentiation of dopaminergic neurons
  • tyrosine hydroyxlase (th): creates precursors of dopamine (L-DOPA specifically)
  • dopamine transporter DAT1 (slc6a3): recycles dopamine
  • vesicular monoamine transporter VMAT2 (slc18a2): membrane protein that transports neuropeptides like dopamine

They found significant decreases in mRNA expression in gdnf, th, slc6a3, and slc18a2 after both acute and chronic administration of 10 mg/kg Ritalin while bdnf was only reduced after chronic 10 mg/kg Ritalin. 

  • Note - mRNA turns into proteins.  It’s like a template that proteins get copied off of.  If there’s less mRNA, there’re fewer proteins that it’s making.

Again, I think it would have been much more interesting had they also included the 1mg/kg dose and those results, even if they were no different than the saline mice.

Evidence for inflammation associated with acute doses of MPH:

They also wanted to see if since there was an increase in activated microglia following the higher dose of Ritalin, they wanted to see whether inflammatory genes had changed expression as well.  Specifically:

  • il-6: signaling protein that is usually activated in burn/tissue damage traumas
  • tnf-alpha: regulates immune cells by inducing fever or even cell death
  • cox-2: causes fevers in response to immune system attack
  • il1b: involved in cell proliferation, cell differentiation and cell death

They found that there were significant increases in mRNA expression of tnf-alpha and il-6 in those given a single dose of 10mg/kg MPH as compared to saline-injected mice.

And these were the results!  Tomorrow we’ll start on the discussion section - which is usually where the researchers talk about why they think they saw what they saw.



Filed under dopaminergic system tymkrs dopamine research chronic ritalin ritalin methylphenidate inflammation gene expression ritalin in mice adhd narcolepsy

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Ritalin and Dopaminergic System Part 3

Still reading through the following article courtesy of @lmcomie:

Sadasivan, S., Pond, B.B., Pani, A.K., Qu, C., Jiao, Y., & Smeyne R.J. (2012) Methylphenidate Exposure Induces Dopamine Neuron Loss and Activation of Microglia in the Basal Ganglia of Mice. PLOSONE, 7(3).

There are more results! Chronic MPH exposure sensitizes the SNpc to MPTP effects:

So since the higher dose of Ritalin (given over 90 days) lowered the dopaminergic neuron number in the substantia nigra, they wanted to see whether it also increased the sensitivity of the neurons to a parkinsonian agent MPTP.  That is, would giving MPTP after Ritalin cause the brain to be more likely to be in a state of stress and would there be additional dopaminergic neuronal death.

  • Reminders: Substantia nigra is a region of the brain involved in reward, addiction, and decreased neuron levels in this area lead to Parkinson’s.
  • MPTP is a neurotoxin precursor to MPP+, which causes permanent symptoms of Parkinson’s disease by destroying dopaminergic neurons in the substantia nigra.

It’s interesting to note that normally these type of mice are not affected by MPTP and do not lose any neurons as a result of receiving this agent.  SO, whichever ones ARE lost, are because of the presence of Ritalin.

So what they found was that giving 1mg/kg or 10mg/kg of Ritalin DID make the neurons more sensitive to MPTP.  That is, where previously they would not have been damaged, they were now.  And MPTP was able to induce a 20% increase in cell death in mice that had RItalin.

They also looked to see how the microglia (cells involved in cleaning/fixing up after a brain injury) reacted to Ritalin and MPTP.  Since only an increase in activated microglia was seen in mice with the higher dose, they only gave this group MPTP (I think they should have given it with the 1mg/kg group as well).  And found that those given 10mg/kg Ritalin + MPTP showed a decrease in the number of resting microglia and a rise in the number of activated microglia.

Note that the increase in dopaminergic neuron loss was not large enough to result in the onset of parkinsonism, but certainly is a factor that should be considered in neurodegenerative disorders that involved the dopaminergic system.


Filed under tymkrs dopaminergic system dopamine neurons mptp mph ritalin chronic ritalin neuroscience

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Ritalin + Dopaminergic System Part 2

I’m currently reading through the following article courtesy of @lmcomie:

Sadasivan, S., Pond, B.B., Pani, A.K., Qu, C., Jiao, Y., & Smeyne R.J. (2012) Methylphenidate Exposure Induces Dopamine Neuron Loss and Activation of Microglia in the Basal Ganglia of Mice. PLOSONE, 7(3).

We just went through the introduction yesterday, and now for results! (Usually methods comes next, but the authors chose to go results first).

Chronic MPH administration affects SNpc DA neuron number:

So we finally hear what they found out.  They looked at the substantia nigra pars compacta, a region of the brain that has been associated with reward, addiction, and degeneration of which is linked to Parkinson’s Disease.  They looked to see what would happen in this region of the brain with chronic exposure (90 days) to saline vs 1mg/kg (ADHD dosage) vs 10 mg/kg (narcolepsy/recreational dosage) - specifically the number of dopaminergic neurons.

They found that for the mice treated with 1mg/kg there was not any difference from the saline (control group) but that in those treated with 10mg/kg for the 90 days had a 20% reduction of dopaminergic neurons in the substantia nigra.  And that it was the neurons towards the back of the substantia nigra that was affected more than those in the front.  The significance of that is (as far as I can tell from a cursory search), still being studied.


The red arrows highlight dopamine neuronal counts for mice with just saline, 1mg/kg, and 10mg/kg Ritalin.  The second graph shows the distance from front to back of the substantia nigra and how many neurons were found in those different sections.

Chronic MPH exposure results in microglia activation in the SNpc:

So as we’ve mentioned a couple of times while reading this study, excess dopamine causes the brain to be in an inflamed and stressed out state.  The scientists wanted to see if chronic Ritalin could induce a reaction similar to that of excess dopamine by measuring the number of resting and active microglia.  

  • Remember that excess dopamine causes release of signaling pepties (cytokines/chemokines) that cause microgliosis (scar formation, new neuron formation, but also production of toxic factors.

What they found was that giving the 1mg/kg (ADHD dose) Ritalin didn’t change any microglia numbers.  And while giving 10mg/kg (narcolepsy dose) Ritalin did not change the number of resting microglia, it did cause a significant increase of activated microglia.  This suggests that there was some form of stress/inflammation occurring, otherwise those microglia would not have activated.


The red arrows point to saline vs 1mg/kg vs 10mg/kg Ritalin.  On the left graph are the resting microglia and the right graph are the activated microglia.  No difference in resting, but statistically significant difference with the 10mg/kg dose of Ritalin.

Dopamine and dopamine turnover affected following chronic MPH dosing:

Then they wanted to see if chronic administration of Ritalin resulted in changes in total striatal dopamine levels or dopamine turnover.

  • Note: The striatum feeds the basal ganglia, all of the parts of the brain that are responsible for control of voluntary motor movements, procedural learning, routine behaviors, eye movements, cognition, and emotion
  • Note: Classically, dopamine turnover is defined as the ratio between dopamine metabolites and dopamine itself.  I think of it as dopamine’s lego-building blocks as opposed to the dopamine itself.  From a quick glance around other articles, an increase in dopamine turnover has been hypothesized to occur early in Parkinson’s disease (PD) as a compensatory mechanism for dopaminergic neuronal loss.  So not a great thing to have, but maybe one of the first lines of defense.  Get rid of the excess dopamine by changing it to its metabolites, save the neuron!

They found that long-term 1mg/kg increased total striatal dopamine compared to saline but that long-term 10mg/kg did not.  And there was a significant increase in major dopamine metabolite named DOPAC at both Ritalin doses.  Luckily (or maybe not) only the 10mg/kg MPH dose saw an increase in dopamine turnover.  So 1mg/kg did not seem to be enough to trigger the dopamine becoming all of its metabolites although there was an increase in DOPAC. (See note after graph)


In looking at the graphs, we can see % dopamine did increase in the 1mg/kg dose but not the 10mg/kg dose.  And that in both 1mg/kg and 10mg/kg doses, there’s an increase in DOPAC.  But it seems that the scientists may have misread graph C because according to this graph, it seems that both 1mg/kg and 10mg/kg MPH have significantly increased turnover as compared to Saline.

I may have to write them asking them! More tomorrow!  (Also this is why it’s important to read the graphs, and not just what is written about them!)


Filed under substantia nigra tymkrs chronic ritalin mph dopaminergic neuron caudal mph exposure microglia activated microglia resting microglia DOPAC dopamine metabolite dopamine turnover neuroscience neuropharmacology

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Ritalin + Dopaminergic System Part 1

Local buddy (though not for long) @lmcomie linked to an interesting article yesterday regarding Ritalin exposure and its effects on the basal ganglial system in mouse models.  So I thought I’d break down the article, and see what all it was saying, but maybe from a more reader-friendly perspective. Here’s the citation and location of the article:

Sadasivan, S., Pond, B.B., Pani, A.K., Qu, C., Jiao, Y., & Smeyne R.J. (2012) Methylphenidate Exposure Induces Dopamine Neuron Loss and Activation of Microglia in the Basal Ganglia of Mice. PLOSONE, 7(3). 


Ritalin has been prescribed for the management of ADHD and narcolepsy.  It’s been shown to be addictive and an increasing number of adults/college students are using it for “cognitive enhancement”.  A number of students feel Ritalin helps them “super-concentrate” so they are using it without regards for why it was brought on the market in the first place.

Previous studies have shown that in both ADHD and non-ADHD populations, Ritalin has been shown to increase scores on tests as well as increase working memory, and people have asked for it to become an over-the-counter drug.  But few studies have been published demonstrating the long-term consequences of using Ritalin.

Ritalin is a stimulant that blocks the dopamine transporter and norepinephrine transporter - much like cocaine.  

  • Note: Transporters are involved in the recycling of signaling neuropeptides.  So when your body signals that dopamine needs to be released, the neurons release them into the gap between neurons known as the synapse.  When they’re done sending the message to the next neuron, transporters vacuum the dopamine back up (or any other neuropeptide), and save them for another day.  So by blocking the dopamine and norepi transporters, you end up with dopamine and norepi staying longer in those synapses, and therefore they act longer on the recipient neurons.

So Ritalin usage leads to an increase in dopamine levels but, be warned, excess levels of dopamine are toxic as it produces superoxide, hydrogen peroxide, and dopamine quinone.  

  • Those are some of the same items that your white blood cells use to kill invading microorganisms.  Great when they’re being controlled by your white blood cells, toxic otherwise.  

Free ranging dopamine has also been shown to cause inflammation to occur in the brain which is shown by an increase in cytokines and chemokines - cell signaling proteins that say “Hey! Brain inflammation going on, take care of it!”  

Microgliosis is one of the processes induced by the increase in these signaling proteins and usually occurs when a person has a brain injury.  It involves microglial cells coming to the site of the injury, getting rid of any germs, getting rid of any dead/damaged neurons, and encourage growth of new neurons.  But, overactivation of the microglial cells leads to production of a number of toxic substances as well as inflammatory factors.

So, this study looks at whether long-term Ritalin usage in mice at 2 doses induces changes in the basal ganglia.  Per wiki, the basal ganglia consists of regions involved in control of voluntary motor movements, procedural learning, routine behaviors, eye movements, cognition, and emotion.  Interesting to note is that the dosages used in the mice - 1mg/kg and 10mg/kg - reflect the prescribed dosages that humans would receive for ADHD and recreational use/narcolepsy (respectively).

  • That is, 1mg/kg = ADHD and 10mg/kg = Narcoplepsy/Recreational 

They looked to see if short term or long term Ritalin changed dopamine neuron numbers and dopamine levels in the substantia nigra portion of the brain.  And since excessive dopamine has been shown to induce inflammation (as mentioned above), they looked to see if after Ritalin, neurons would be more sensitive to a drug MPTP that has been shown to cause neuron damage.

  • Note: substantia nigra is a portion of the brain that plays a role in reward, addiction, and movement.  Loss of dopaminergic neurons in this area leads to Parkinson’s Disease.

Results tomorrow!


Filed under tymkrs substantia nigra dopamine dopaminergic system ritalin methylphenidate chronic ritalin transporters neuropeptides neuroscience